Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, January 15, 2017

Glia, Not Neurons, Most Affected By Brain Aging

You just aged/lost 5 years of your brain due to your stroke. What protocols does your doctor have to catch back up?
http://neurosciencenews.com/glia-brain-aging-5902/

The difference between an old brain and a young brain isn’t so much the number of neurons but the presence and function of supporting cells called glia. In Cell Reports on January 10, researchers who examined postmortem brain samples from 480 individuals ranging in age from 16 to 106 found that the state of someone’s glia is so consistent through the years that it can be used to predict someone’s age. The work lays the foundation to better understand glia’s role in late-in-life brain disease.
“We extensively characterized aging-altered gene expression changes across 10 human brain regions and found that, in fact, glial cells experience bigger changes than neurons,” says Jernej Ule, a neurobiologist at the Francis Crick Institute and the University College London, who led the study with departmental colleague Rickie Patani and first author Lilach Soreq. “There’s quite a bit of regional information that will be of interest to different people–for example some will notice a very unique pattern of astrocyte-specific changes in the substantia nigra–and we provide a lot of data that still needs to be analyzed.”
There are three types of glia cells, each providing different kinds of support to neurons: oligodendrocytes insulate, microglia act as immune cells, and astrocytes help with neuron metabolism, detoxification, among many functions. Based on analysis of human brain tissue samples, primarily from the UK Brain Expression Consortium, the researchers show that astrocytes and oligodendrocytes shift their regional gene expression patterns upon aging, (e.g., which genes are turned on or off) particularly in the hippocampus and substantia nigra–important brain regions for memory and movement, respectively–while the expression of microglia-specific genes increases in all brain regions.
The investigators next took a preliminary look at whether these changes in gene expression could relate to changes in brain cell populations. Based on a comparison of tissue samples from 3 young and 3 old brains, they found that the number of oligodendrocytes decreases with age in the frontal cortex. They further established that this likely corresponds with decreased expression of oligodendrocyte specific genes. Other types of cells had more complicated patterns of change.
This graphic depicts the numbers and function of glia and neurons in the aging human brain.
This graphic depicts the numbers and function of glia and neurons in the aging human brain. NeuroscienceNews.com image is credited to Lilach Soreq.
“We developed a very nice machine learning program and had to go through hundreds of thousands of oligodendrocytes and neurons to get reliable data, but we wanted to understand whether decreased expression causes changes at the molecular or cellular-level,” Ule says. “We did see oligodendrocytes disappearing but with neurons we didn’t see dramatic changes in cellular numbers except for a decrease in the largest neurons. This is of interest because those largest neurons are generally connected to neurodegenerative diseases.”
One unexpected finding was that certain glial gene expression patterns could predict age in the general population. While this can only be done postmortem, and certain people will not fit neatly into these patterns, it does provide scientists one more tool to understand how aging in the brain may be linked to the causes of age-related disorders. The researchers’ ultimate goal is to see whether gene mutations or other variables could affect gene expression in ways that cause disease.
About this neuroscience research article
Funding: This work was supported by the European Research Council; the Marie Curie Intra European Fellowship and Alzheimer’s Society for Junior Investigator award, the Francis Crick Institute, the UK Medical Research Council, the Wellcome Trust; the UK Medical Research Council; and the US National Institute on Aging, NIH.
Source: Joseph Caputo – Cell Press
Image Source: NeuroscienceNews.com image is credited to Lilach Soreq.
Original Research: Full open access research for “Major Shifts in Glial Regional Identity Are a Transcriptional Hallmark of Human Brain Aging” by Lilach Soreq, UK Brain Expression Consortium, North American Brain Expression Consortium, Jamie Rose, Eyal Soreq, John Hardy, Daniah Trabzuni, Mark R. Cookson, Colin Smith, Mina Ryten, Rickie Patani, and Jernej Ule in Cell Reports. Published online January 10 2017 doi:10.1016/j.celrep.2016.12.011
Cite This NeuroscienceNews.com Article

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